SACCM 17: Hypoventilation Flashcards
What are 3 categories of causes for hypercapnia?
- hypoventilation
- increased CO2 production e.g., fever
- increased dead space
Minute ventilation equation
VE = VT x RR
Alveolar ventilation equation
VA = VE - VD
Tidal volume equation
VT = VD + VA
What is the location of the anatomic dead space?
respiratory system down to the level of the terminal bronchioles
What is alveolar dead space?
part of the alveoli that is ventilated but does not participate in gas exchange/not perfused
< 5% normally
What is the physiologic dead space?
sum of anatomic and alveolar dead space
How do you determine anatomic dead space?
Fowler’s method
measures exhaled nitrogen after giving breath with 100% O2 -> nitrogen cc graphically displayed over time against volume exhaled
-> can derive dead space from this graph
How can you calculate physiologic dead space in a clinical setting
Enghoff modification of the Bohr equation
Explain the Bohr equation for physiologic dead space and its limitations
concept: CO2 comes from airway participating in gas exchange (i.e., not dead space) -> alveolar versus expired CO2 difference should demonstrate dead space
VT x FECO2 = (VT - VD) x FACO2 -> rearrange to:
VD/VT = (FACO2 - FECO2) / FACO2
limitations: FACO2 difficult to measure and alveolar CO2 different in part of lungs
Explain how the Enghoff modification is applied and what are its limitations
Alveolar CO2 difficult to measure -> PaCO2 as surrogate -> mixed product of all lung fields -> more representative of average CO2 of all alveoli
VD/VT = (PaCO2 - ETCO2) / PaCO2
limitations: influenced by reasons for PaCO2 - PACO2 gap, e.g., diffusion impairment, intrapulmonary shunt, V/Q mismatch
how do you determine the alveolar dead space
substract the Fowler (anatomic) dead space from the Bohr/Enghoff (physiologic) dead space
PACO2 is directly proportional to ________ and inversely proportional to __________
PACO2 is directly proportional to PACO2 produced and delivered to lungs and inversely proportional to alveolar ventilation
What PaCO2 levels are consistent with hyper- or hypoventilation
hyperventilation < 30-35 mm Hg
hypoventilation > 40-45 mm Hg
How does PvCO2 compare to PaCO2?
PvCO2 generally 3-6 mm Hg higher than PaCO2
Name 5 examples of causes for increased inspired CO2
- faulty breathing circuits
- excess apparatus dead space
- inadeqaute fresh gas flow
- exhausted absorbent
- faulty unidirectional valves
Name 6 examples for increased CO2 production
- fever
- sepsis
- thyrotoxicosis
- malignant hyperthermia
- overfeeding
- exercise
why does increased CO2 production rarely lead to hypercapnia?
because minute ventilation changes can usually compensate for this increaed production -> will exhale more CO2
If an animal’s tidal volume decreases and it normalizes its VE by increasing the RR, how can this still lead to hypercapnia?
decreaes tidal volume -> anatomic dead space volume won’t change -> proportion of alveolar ventilation will be smaller and this will not change even with increased RR
-> higher proportion of VD/VT possible even with normal VE
What should you suspect when your patient has hypercapnia with increased arterial to end-tidal CO2 gradient but increased VE?
suspect increased alveolar dead space/ventilation of poorly or not perfused alveoli
e.g.,
* PTE
* Pulmonary capillary compression from pulmonary overinflation
* cardiovascular shock
What are the cardiovascular effects of hypercapnia?
- CO2 decreases myocardial contractility and SVR
Why are the systemic cardiovascular effects of hypercapnia rarely clinically apparent?
concurrent increase in sympathetic tone and catecholamine release -> increased HR and vasoconstriction
What are the effects of hypercapnia on the pulmonary/respiratory system?
- vasoconstriction of the pulmonary circulation
- bronchodilation
- decreaed diaphragmatic contractility
Explain the neurologic effects of hypercapnia
- cerebral vasodilation -> increased cerebral blood flow -> increased intracranial pressure -> altered consciousness, seizures, altered brainstem reflexes and portural/motor responses
- CO2 narcosis from intracellular pH changes and cellular metabolism alterations
At what PaCO2 can CO2 narcosis develop?
PaCO2 > 90 mm Hg
How can hypercapnia lead to AKI?
causes constriction of the renal afferent arteriole
What leads to a leftward shift of the oxyhemoglobin dissociation curve?
- decreased temperature
- decreased PaCO2
- increased pH
- decreased 2,3-DPG
What leads to a rightwards shift of the oxyhemoglobin dissociation curve?
- increased temperature
- decreased pH
- increase PaCO2
- increase 2,3-DPG
How is CO2 carried in venous blood (name fraction of CO2 in % for each mechanism)
- dissolved in plasma (10%)
- buffered within RBCs as bicarbonate (90%)
What are the 2 reasons PvCO2 increaes in states of decreased tissue perfusion?
- accumulation of CO2 in underperfused tissue beds
- anaerobic metabolism -> lactate production and hydrolysis of ATP -> increaed H+ production -> will be buffered by HCO3- -> CO2 production
what is the normal PaCO2 to ETCO2 gradient?
ETCO2 2-6 mm Hg lower than PaCO2
Name the 3 mechanisms by which O2 treatment in chronically hypoventilating patients causes worsening of hypercapnia
- depression of hypoxia driven chemoreceptors (rely more on peripheral O2 sensitive chemreceptors)
- relief of hypoxic pulmonary vasoconstriction -> increased perfusion without concomitant increased ventilation (low V/Q)
- increased Hb O2 saturation -> less CO2 carrying capacities (Haldane effect)
What is the currently recommended target PaO2 and SpO2 in chronically hypoventilating patients
PaO2 60-70 mm Hg
SpO2 90-93%
Name 5 examples for respiratory stimulants
- doxapram
- aminophylline
- theophylline
- caffeine
- progesterone
